Journal: Signal Transduction and Targeted Therapy

Article Title: Pulsed electromagnetic fields inhibit atherosclerosis by regulating pyroptosis through membrane tension-mediated mechanosensitive channels

doi: 10.1038/s41392-025-02479-2

Figure Lengend Snippet: PEMFs inhibit the formation of atherosclerotic plaques by attenuating pyroptosis and inflammation. a Oil red O staining was used to determine the lesion burden in the aorta in the ApoE-/- mouse groups: the normal chow diet (ND) group, high-fat diet (HFD, 15 weeks) group, and HFD+PEMFs (15 Hz, 1.5 mT, 1 h/day, 3 weeks) group; n = 5 mice per group. b Evans blue staining was used to assess aortic permeability under the same experimental conditions; n = 5 mice per group. Scale bar = 100 μm. c , d HE staining was used to visualize the plaque area (yellow arrows) in the aortic arch, and the results were quantified; n = 5 mice per group. Scale bar = 100 μm. e , f Serum levels of IL-1β and IL-18 were detected by ELISA; n = 5 mice per group. g Pyroptosis was assessed by flow cytometry via Hoechst 33342/PI staining in MVECs. h Western blot analysis of NLRP3, ASC, p20 caspase-1, and GSDMD-NT in aortic tissues; n = 5 mice per group. i Untargeted lipidomic analysis of aortic tissues from all experimental groups. KEGG pathway analysis of the top 10 differential lipids between the HFD + PEMF and HFD groups. Dots represent metabolites (blue: downregulated; red: upregulated). The pathway descriptions are described as follows: mmu00564: Glycerophospholipid metabolism; mmu00600: Sphingolipid metabolism; mmu04979: Cholesterol metabolism; mmu05231: Choline metabolism in cancer; mmu04975: Fat digestion and absorption; mmu04071: Sphingolipid signaling pathway; mmu04136: Autophagy–other; mmu04931: Insulin resistance; mmu00563: Glycosylphosphatidylinositol (GPI)−anchor biosynthesis; mmu04714: Thermogenesis; n = 5 mice per group. j Hierarchical clustering of the top 20 significantly altered lipids between the HFD + PEMF group and the HFD group, classified by LIPID MAPS: GL (glycerolipid), SP (sphingolipid), and GP (glycerophospholipid), n = 5 mice per group. k Double immunostaining of NLRP3 and CD31 in atherosclerotic lesions among different groups of mice; n = 5 mice per group. Scale bar = 100 μm. l Manders’ coefficient was used to evaluate the NLRP3-positive area within CD31-positive regions in the aortic arch plaques; n = 5 mice per group. m Quantitative comparison of NLRP3 colocalization with CD31 (ECs) and CD68 (macrophages) in the same mice; n = 5 mice per group. All the data represent biological replicates. The measured data are presented as the mean ± SEM. Statistical significance was assessed by one-way ANOVA with Tukey’s multiple comparison test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: Untargeted lipidomics and analysis were performed by Shanghai Bioprofile Technology.

Techniques: Staining, Permeability, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Western Blot, Double Immunostaining, Comparison

Journal: Cancer Biology & Therapy

Article Title: Loss of ACSL1 fuels ferroptosis resistance in clear cell renal carcinoma

doi: 10.1080/15384047.2025.2567815

Figure Lengend Snippet: In vivo validation of ACSL1 to promote ferroptosis in ccRCC xenografts. (A) Detection and statistical analysis of the ferroptosis marker proteins SLC7A11 and GPX4 in xenografts overexpressing ACSL1. (B) Measurements of Fe²⁺, MDA, and GSH levels in xenograft tissues. (C) ROS and C11-BODIPY levels in frozen xenograft sections were assessed by fluorescent probes, with quantitative analysis. Scale bar = 50 μm. (D, E) Untargeted lipidomics analysis showing significant elevation of PE species containing arachidonic acid (C20:4) or adrenic acid (C22:4) in the OE group under negative-ion (D) and positive-ion (E) modes. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The untargeted lipidomics analysis was conducted by Novogene Co., Ltd. (Beijing, China).

Techniques: In Vivo, Biomarker Discovery, Marker